Transfected Stable Cell Lines
Reliable | High-Performance | Wide Rage
Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
Cat. No. : CSC-SC000262
Host Cell : HEK293 (CHO and other cell types are also available) Size : >1x106 frozen cells/vial
| Cat. No. | CSC-SC000262 |
| Description | Using Creative Biogene's proprietary lentiviral vectors, we subclone the target gene into lentivector, generate the lentivirus particles, sequentially infect the cell line HEK293 (other cell types are also available according to your requirements), and select the clones constantly expressing target gene at high level. |
| Target Gene | ADAMTS5 |
| Gene Species | Homo sapiens (Human) |
| Host Cell | HEK293 (CHO and other cell types are also available) |
| Host Cell Species | Species varies |
| Applications |
1. Gene expression studies 2. Signaling pathway research 3. Drug screening and toxicology 4. Disease research |
| Size | 2 × 10^6 cells / vial |
| Stability | Validated for at least 10 passages |
| Quality Control | Negative for bacteria, yeast, fungi and mycoplasma. |
| Storage | Liquid nitrogen |
| Shipping | Dry Ice |
| Revival | Rapidly thaw cells in a 37°C water bath. Transfer contents into a tube containing pre-warmed media. Centrifuge cells and seed into a 25 cm2 flask containing pre-warmed media. |
| Mycoplasma | Negative |
| Format | One frozen vial containing millions of cells |
| Storage | Liquid nitrogen |
| Safety Considerations |
The following safety precautions should be observed. 1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum. 2. No eating, drinking or smoking while handling the stable line. 3. Wash hands after handling the stable line and before leaving the lab. 4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells. 5. All waste should be considered hazardous. 6. Dispose of all liquid waste after each experiment and treat with bleach. |
| Ship | Dry ice |
| Gene Name | ADAMTS5 ADAM metallopeptidase with thrombospondin type 1 motif, 5 [ Homo sapiens ] |
| Gene Symbol | ADAMTS5 |
| Synonyms | ADMP-2; ADAM-TS5; ADAMTS-5; ADAMTS11; ADAM-TS 5; ADAMTS-11; ADAM-TS 11 |
| Gene ID | 11096 |
| Uni Prot ID | Q9UNA0 |
| m RNA Refseq | NM_007038.3 |
| Protein Refseq | NP_008969.2 |
| Chromosome Location | 21q21.3 |
| Function | integrin binding; metalloendopeptidase activity; metallopeptidase activity; protein binding; zinc ion binding; |
| Pathway | Endochondral Ossification, organism-specific biosystem; |
| MIM | 605007 |
Helicobacter pylori (H. pylori) is a Group 1 carcinogen that can induce gastric cancer (GC). Here, researchers screened for a regulatory axis with the highest correlation coefficient: lncRNA (MSTRG.10627.1)-miRNA (miR-142-5p)-mRNA (ADAMTS5). They also validated the combinations of MSTRG.10627.1 and miR-142-5p, and miR-142-5p and ADAMTS5. H. pylori can downregulate ADAMTS5 expression. Downregulation of ADAMTS5 expression promotes the proliferation, migration, and invasion of gastric cancer cells; while overexpression of ADAMTS5 inhibits these processes. Silencing ADAMTS5 in gastric cancer cell lines showed increased PI3K protein expression and AKT protein phosphorylation levels, and suppressed expression of the tumor suppressor gene p53. However, overexpression of ADAMTS5 in gastric cancer cells produced the opposite results. Results from a nude mouse subcutaneous tumor model showed that silencing ADAMTS5 increased tumor weight and volume. In a metastatic tumor model, overexpression of ADAMTS5 inhibited gastric cancer cell metastasis. These studies suggest that Helicobacter pylori may downregulate ADAMTS5 expression through a pathway (MSTRG.10627.1-miR-142-5p-ADAMTS5). Furthermore, downregulation of ADAMTS5 induces PI3K protein expression, upregulates phosphorylated AKT protein, and downregulates p53, which plays an important role in the development and progression of gastric cancer.
When ADAMTS5 expression was disrupted, the rate of cell scratch healing accelerated (Figure 1a). Cell scratch assays showed that the scratch healing rate was significantly reduced in the ADAMTS5 overexpression group compared to the empty vector group (Figure 1b, c). Transwell assays showed that when ADAMTS5 expression was disrupted, the number of cells crossing the superior chamber membrane and matrix gel significantly increased (Figure 1d, e). Compared to control cells, the number of cells crossing the superior chamber membrane and matrix gel in the ADAMTS5 overexpression group was reduced (Figure 1f-i). These results indicate that ADAMTS5 significantly inhibits the migration and invasion of gastric cancer cells and may be involved in regulating gastric cancer cell metastasis.
Figure 1. The effects of ADAMTS5 on the migration and invasion of GC cell lines. (Yin Z, et al., 2026)
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